Tokuue J, Hayashi J, Hata Y, Nakahara K, Ikeda Y
Department of Medicine and Gerontology, Kyorin University, Tokyo, Japan.
Thromb Haemost. 1996 May;75(5):833-7.
Platelet activation induced by shear forces occurring in a stenosed coronary artery is one of the mechanisms of coronary thrombosis. We evaluated the shear-induced platelet aggregation (SIPA) dynamics in patients with effort angina during treadmill exercise. SIPA was measured by a rotational cone-plate aggregometer. SIPA was markedly increased by exercise from 71.2 +/- 8.9% to 81.9 +/- 7.6% (p < 0.01) in the patient group. Although epinephrine concentrations were elevated, its rate of increase was not correlated with that of SIPA. Yohimbine partially inhibited the exercise-induced increase in SIPA. In contrast, a significant correlation between the changing rate of plasma von Willebrand factor (vWF) larger multimers and that of SIPA (r = 0.74, p < 0.05) was observed. Exercise-augmented SIPA is probably dependent on an increase in vWF larger multimers rather than platelet alpha2-receptor activation. Prevention of the interaction between vWF and its platelet receptors may play some role in decreasing the risk of coronary thrombosis during exercise.
在狭窄冠状动脉中由剪切力诱导的血小板活化是冠状动脉血栓形成的机制之一。我们评估了运动性心绞痛患者在跑步机运动期间剪切诱导的血小板聚集（SIPA）动态变化。通过旋转锥板式聚集仪测量SIPA。在患者组中，运动使SIPA从71.2±8.9%显著增加至81.9±7.6%（p<0.01）。虽然肾上腺素浓度升高，但其增加速率与SIPA的增加速率不相关。育亨宾部分抑制运动诱导的SIPA增加。相反，观察到血浆血管性血友病因子（vWF）较大多聚体的变化率与SIPA的变化率之间存在显著相关性（r = 0.74，p<0.05）。运动增强的SIPA可能依赖于vWF较大多聚体的增加，而不是血小板α2受体的激活。预防vWF与其血小板受体之间的相互作用可能在降低运动期间冠状动脉血栓形成风险中发挥一定作用。
